Cardiac Cycle and Special Circulations Flashcards
when do heart valves produce a sound
when they shut
what is the blood flow across the heart
SVC-RA-TV-RV-PV-PA-PV-LA-MV-LV-AV-A
what triggers the recurring cardiac cycleof atrial and ventricular contractions and relaxations
the orderly depolarisation/ repolarisation sequence
what is the cardiac cycle composed of
all events from one heart beat to the next
describe heart in diastole
heart ventricle are relaxed and fill with blood
describe the heart in systole
heart ventricles contract and pump blood into the aorta (LV) and pulmonary artery (RV)
which side of the heart has a lower pressure
left
what are the 5 main events during the cardiac cycle
passive filling, atrial contraction, isovolumetric contraction, ventricular ejection, isovolumetric ventricular relaxation
after what does the valve close and why
Isovolumetric ventricular Contraction- so volume of blood stays the same
what happens to the mitral valves during ventricular ejection
stays closed as blood is ejected into aorta
what happens to the valves during isovolumetric relaxation
both closed and ventricle relaxes around volume of blood
what allows passive filling
pressure gradient between artia and ventricle (both close to 0)
what fills majority of ventricle
80% passive filling, 20% contraction
what does the P wave in the ECG signal
atrial depolarisation
when does the artria contract in the ECG
between the P wave and QRS
what completes the end diastolic volume
atrial contraction
when does ventricular contraction start in the ECG
after the QRS (signals ventricular depolarisation)
what causes the AV valves to shut
when the ventricular pressure exceeds the atrial pressure
what causes the LUB sound
AV valve shutting
describe isovolumetric contraction
tension rises around a closed volume
when does the aortic/pulmonary valve open causing ventricular ejection
when ventricular pressure exceeds aorta/pulmonary artery pressure
what does the T wave on the ECG signal
ventricular repolarisation
what happens to the ventricles after the T wave
relax and the ventricular pressure starts to fall
when do the aortic/ pulmonary valves shut after ventricular ejection
when ventricular pressure falls below aortic / pulmonary pressure
what produces the secondary heart sound (DUB)
closure of aortic/ pulmonary valves after ventricular ejection
what does the valve vibration produce in the aortic pressure curve
dicrotic notch
what does closure of aortic/and pulmonary valves signals the start of
isovolumetric ventricular relaxation
describe the AV valves during isovolumetric ventricular relaxation
shur, tension falls around a closed volume
when do AV valves reopen after isovolumetric ventricular relaxation
When the ventricular pressure falls below atrial pressure
what does the first heart sound signal the beginning of
systole
what does the second heart sound signal the beginning of
diastole
why does arterial pressure never fall to zero
as arteries stretch and recoil
when does the JVP occur
after right atrial pressure waves
what type of pulse is JVP
wave pulse
where do the coronary arteries arise from
the base of the aorta
where does the majority of the venous blood drain from the heart into and via what
goes into right atrium via coronary sinus
what are the special adaptations of the coronary circulation
high capillary density
high basal blood flow
high oxygen extraction under resting conditions
what does the high level of oxygen extraction by the myocardium mean for changes in oxygen requirements
only way to increase oxygen supply to heart is to increase coronary blood flow
what controls coronary blood flow
intrinsic and extrinsic mechanisms
how do intrinsic mechanisms control coronary blood flow
decrease PO2 causes vasodilatation of coronary arterioles in attempt to supply heart with more blood
metabolic hyperaemia
adenosine (produced from breakdown of ATP) is a potent vasodilator
what intrinsic mechanisms control coronary blood flow
supplied by sympathetic vasoconstrictors
BUT
over ridden by metabolic hyperaemia (as a result of increase HR and SV)
symp stim results in coronary vasodilatation
adrenaline activates beta 2 adrenergic receptors cause vasodilatation and increased blood supply
what does stimulation of alpha receptors do
vasoconstriction
what what stimulation of beta 2 receptors do
vasodilatation
what stimulates beta 2 receptors
circulating adrenaline
how does decreased PO2 affect adenonsine and therefore coronary blood flow
increases adenosine and increases blood flow
how does an increase of metabolites affect coronary blood flow (K+, PCO2, H+)
increases blood flow
when does peak left coronary flow occurs and why
diastole
During contraction of the ventricular myocardium (systole), the subendocardial coronary vessels (the vessels that enter the myocardium) are compressed due to the high ventricular pressures. This compression results in momentary retrograde blood flow (i.e., blood flows backward toward the aorta) which further inhibits perfusion of myocardium during systole
what happens to blood supply to the heart if you shorten diastole
decreases, coronary blood flow highest in diastole
why are the right coronary arteries less affected by contractions of the ventricles/ atrium
as right side doesn’t contract as much
when does most myocardial perfusion occur
in diastole when the subendocardial vessels from the left coronary artery are not compressed
what arteries supply the brain
internal carotids and vertebral arteries
what happens if the grey matter of the brain is starved of oxygen
consciousness lost after few seconds of ischaemia, irreversible cell damage within ~ 3 minutes
what is the circle of willis
basilar (2 vertebral arteries) and carotid arteries anastomose to form circle of willis (vessel ring at base of brain)
what arises from the circle of willis
major cerebral arteries
do brain arteries respond to the barorecptor reflex
not necessarily
what causes a stroke
interruption/ cut off of blood supply to a region of the brian
what do auto regulation do and in what ranges does it work
autoregulation of cerebral blood flow guards against changes in blood flow if mean arterial blood pressure changes (between 60-160mmHg)
does sympathetic stimulation have a big effect on cerebral blood flow
no has little effect
due to autoregulation what happens to resistance vessels if MABP rises
constrict to limit blood flow
due to autoregulation what happens to resistance vessels if MABP fall
dilate to maintain bloodflow
what does a MABP below 50 mmHg cause
confusion, fainting and brain damage
what effect does increased PCO2 have on the cerebral vessels
causes vasodilatation
what effect does decreased PCO2 have on the cerebral vessels
causes vasoconstriction
what is regional hyperaemia
blood flow increases to active parts of the brain
what is ICP and its normal values
intracranial pressure 8-13 mmHg
what is CPP and how is it calculated
cerebral perfusion pressure (MAP - ICP)
what effects does an increasing ICP have on CPP and cerebral blood flow
decreases CPP and cerebral blood flow
what can increase ICP
head injury or brain tumour
what is the blood brain barriers
cerebral capillaries which have very tight intercellular junctions
what are cerebral capillaries highly permeable to
O2 and CO2
how does glucose pass the BBB
by facilitated diffusion using specific carrier molecules
what is the BBB exceptionally impermeable to , what does this allow
hydrophilic substances such as ions, catecholamines, proteins etc
helps protect brain neurones from fluctuating levels of ions etc in blood
how much of cardiac output travels into pulmonary circulation from the right ventricle
all of it
what meets the metabolic needs to the airways
systemic bronchial circulation
how much of systemic circulation resistance is pulmonary
about 10%
how does pulmonary capillary resistance compare to systemic capillary resistance
low
what adaptation of the pulmonary circulation helps to protect against pulmonary oedema
absorptive forces
what effect does hypoxia have on pulmonary arterioles
vasoconstriction- opposite so that blood is diverted away from poorly ventilated areas of lung
what is resting blood flow low
because of sympathetic vasoconstrictor tone
what overcomes sympathetic vasoconstrictor activity during activity
metabolic hyperaemia
what changes in the vasculature occur during exercise
blood flow to skeletal muscle increases
Metabolic hyperaemia overcomes sympathetic vasoconstrictor activity
Circulating adrenaline causes vasodilatation (beta2 adrenergic receptors)
Plus increased cardiac output during exercise, these could increase skeletal muscle blood flow many folds
where do large veins in limbs lie
between skeletal muscle
what causes varicose veins
blood pooling in the lower limbs if venous valves become incompetent
why do varicose veins lead to reduce cardiac output
because of chronic compensatory increase in blood volume
